Thursday, July 28, 2011

It happens every six months or so, a news article picks up on a new miraculous cure involving marijuana and I start this argument all over again. On one side is usually a group advocating legalization using medical marijuana as justification. On the other side are strict traditionalists claiming that there are no medicinal benefits, and the legalizers just want an excuse to smoke pot. So where does that leave the scientists and doctors who are actually doing research into the medicinal applications of cannabinoids (the chemical ingredients of the cannabis sativa marijuana plant)?

Well, usually in the middle. And as is true in so many cases, the efforts to identify and bring to practice real medicinal uses are hurt by both sides.

First and foremost, I am not arguing for or against legalization. I really don't care that much what substances you put into your body. Legalization is a question to be decided by a society that debates and votes for their respective stand on the issue. As a researcher of cannabinoids I have a stake only in potential medicinal applications – but also in the use and mis-use of the concept of medical marijuana.

I do not find marijuana to be harmless. There are side-effects. Cannabinoids alter memory, they alter the ability to make critical decisions, in some cases they can affect reaction time, and smoking the unprocessed, unfiltered leaf exposes the lungs to more chemicals than tobacco. It can reveal latent tendency to anxiety, depression or schizophrenia. It is up to society to decide if those side-effects are less than, say, ethanol. This is why I stay out of the legalization argument.

Where I do argue is against the use of "marijuana" as a medicinal agent. There are very few medical applications where smoking marijuana is an appropriate means of delivering appropriate cannabinoids to the body. One of those is cancer pain – by all means, if the marijuana alleviates pain and allows the patient to escape for a few hours, do it.

But there are many other medicinal applications: glaucoma, nausea, loss of appetite due to chemotherapy, bone pain, convulsions, stress, cancer, and now… autism (http://www.ksdk.com/news/article/267091/9/Using-medical-marijuana-to-treat-autism). The recent autism reports are disturbing because there is no research supporting the results, and the probable mechanisms would likely be from compounds other than the widely known ingredients of marijuana. The problem is that so many of these medicinal applications do not rely on the same chemical compounds of marijuana smoke. Smoking marijuana bought from a street vendor – whether a medicinal storefront in Berkeley or a street pusher in Detroit – provides no control over the chemical constituents of marijuana.

Does that matter? In a word – yes. The chemical compounds mean everything with respect to effects. You've probably heard of Tetrahydrocannabinol – THC – the main ingredient of marijuana. But did you know that there is more than one type of THC? There's Delta-9-THC. That's the one usually referred to with marijuana, but there's also Delta-8-THC and 11-hydroxy-THC. Those are slightly different chemical compounds, and have slightly different potencies. How about Cannabidiol? Ever hear of it? Cannabidiol is responsible for some of the anticonvulsive and anti-anxiety effects of marijuana. How about Cannabigerol, Cannabidivarin or Tetrahydrocannabivarin? These are all trace ingredients on the average in the cannabis sativa plant. New research shows that these compounds have some very important medicinal effects – as well as potential side effects depending on what is being treated.

And here's the dirty little secret of medical marijuana – when buying street pot, you don't know how much of these other chemicals are in the plant. Pot is grown – even bred like roses and show dogs – for a particular characteristic, the euphoric feeling or "high." Cannabindiol for one, and some of the other cannabinoids block or reduce that high. About one third of all pot available in the U.S. has negligible Cannabidiol. Now if you were counting on that "medicinal" effect, you're out of luck!

The concept of buying pot from any source and self-medicating is not medicine – it's smoking pot. Pot smoking is not medicinal. If you go to the doctor with severe pain, he doesn't prescribe chewing tree bark (for salicylate, the main ingredient in aspirin), boiling poppies (for opium and its primary product, morphine) or eating mushrooms (for muscarine, and it's derivative acetylcholine). No, the doctor prescribes a controlled dose of a drug that is a purified chemical derived from or synthesized to resemble a single ingredient in those substances. Again, medical marijuana, as practiced in this manner is not medicinal.

I once had this argument online in a discussion group and my opponent started listing research studies that proved the medicinal benefits of marijuana. Yes, there are studies that support medicinal applications. However, my favorite was an article that showed suppression of lymphoma growth: Marijuana Cures Cancer! Unfortunately not true. The discussion stopped cold when I pointed out that the substance used in the test was a synthetic chemical (first identified in Israel where they do a lot of medicinal cannabinoids research) and was not present in the cannabis plant and therefore could never be obtained by medical pot smoking!

At the recent meeting of the International Cannabinoid Research Society – a group of about 400 scientists and physicians that study cannabis and cannabinoids from drug abuse to medicinal potential – less than 10% of the scientific presentations used smoked marijuana – and most of those were abuse studies. The truly medicinal studies used purified extracts and synthetic compounds. Here's a hint: if an article refers to THC it is probably talking about marijuana leaf or at least a purified extract; if it mentions cannabidiol (CBD) is definitely a purified extract; if it mentions chemical designations such as WIN 55212-2, CP55940, HU-210, anandamide, 2-AG, it is talking about synthetic compounds not found in marijuana.

In summary, I really don't have much of a stand on marijuana legalization, but I oppose medical marijuana use as it is currently practiced in this country. Why? Because it is not medicinal. It is becoming more obvious that there are many medicinal benefits to be had from a better study of the cannabinoid chemicals in cannabis. Those benefits are all too easily confused by those who promote use of a drug in the absence of controlled dosing, known chemical composition and physician monitoring. To argue otherwise is contrary to decades of scientific research attempting to understand those medical applications.

Smoke pot, or not. Just leave so-called "medical" pot smoking out of the debate.

[Dr. Tedd "Speaker to Lab Animals" Roberts is a neuroscientist with 29 years research experience studying effects of drugs on learning, memory and cognitive decision making in animals and humans.]

In the previous series of blogs from The LabRats Guide to the Brain,I mentioned that many surgical treatments have been used to remove the neural tissue that acts as a site of origin for epileptic seizures. One of the pioneers of this work was Dr. Wilder Penfield, who has been mentioned in this blog in the past (click on the content tags for previous blogs). Penfield's medical research involved identifying the point of origin for epileptic activity, then surgically removing that piece of the brain. Before the surgery, however, Penfield and colleagues need to find out what function is served by that area of brain. Very low voltage/amperage electrical stimulation was delivered via hair-thin stimulating electrodes. Clearly some stimulations caused physical body movement, and unfortunately some triggered the very epileptic activity being treated. But some of the other results were astounding: patients described sensations, feelings or complete memories. These studies gave rise to much of the mapping that we know today - including that of the motor and sensory homunculi are courtesy of such recordings as preparation for epilepsy surgery.

Another striking result of epilepsy surgery was the case of patient H.M., very well known to neurosurgery and neuroscience students alike. H.M.s epilepsy originated in the hippocampus, an area near and dear to my... memory. Yes, the hippocampus is the structure most associated with processing of new memories. On September 1, 1953, neurosurgeon William Beecher Scoville removed part of the medial Temporal Lobe on both sides of H.M.'s brain. From that point onward, his ability to form new memories was impaired, although his ability to learns skills and remember past events appeared unaffected. The surgery removed most of the hippocampus, amygdala and entorhinal cortex, thus removing a critical link in the brain circuitry necessary for processing memory. H.M. died in 2008, and for 55 years he became the most studied patient in Neuroscience!

Another strange but true tale involves the split-brain. Epileptic seizures can originate in a small area of brain and eventually spread to involve major portions of both hemispheres. As a last-chance attempt to halt the progress to the opposite hemisphere and limit the duration and extent of seizure, a procedure called corpus callosotomy is performed to cut the connections between hemispheres of the brain. The resulting separation resulted in much of what we now understand to be the lateralization of functions to two different halves of the brain. However, it is the behavior of the "split-brain" patients that is most curious. As discussed in the sections on vision, each retina projects the left half of the visual field to the right brain, and the right half of the field to the left brain. Without an intact corpus callosum connecting the two hemispheres, the patient cannot put both halves of the visual field together. As a result, they constantly scan their eyes back and forth and move their head to allow both halves of the brain to "see" the entire field. Split-brain patients have been observed to be in conflict between intended actions controlled by the separate halves of the brain - expressed as one handing restraining or slapping the other, or two hands attempting to do the same task.

Fortunately these drastic surgeries not performed with much frequency, rather medication and more precise surgical techniques suffice for most epilepsy patients. Still, drastic cases exist, and parts of the brain may need to be removed. The resulting responses, deficits, and conflicts are very important to our understanding of the brain!

Until next time - take care of your brain - you don't want to lose it!

Monday, July 25, 2011

Sidney Harris has been drawing cartoons that poke fun at - and point out the limitations of - sceince for a long time. Sidney's work shows up in all of the science labs sooner or later - in fact, his work is about on par with Gary Larson's The Far Side* in terms of showing up on lab doors, walls, offices, etc.

Today's link is to a comic which tickles my funny bone since it actually hits pretty close to home. When you train a lab rat to perform a particular test, it will get better at that test. Then you have to come up with a harder test. Pretty soon the rat gets good at that test...

Be sure to go back to the home page and check out more of Sidney Harris' cartoons.
*Now for that Two-fer.

Here's one of those Far Side cartoons that I have seen in many labs:

Anyone who has ever worked with old equipment in a lab has probably felt like they were working with one of these "early microscopes." I had one about 20 years ago that looked pretty much the same. Of course it was already 20 years old by that time.

I have noticed that labs that do not have the latest and best equipment and devices - that have to scrimp and save and do their own maintenance - tend to have this cartoon up somewhere.

Been there, done that.

And for the sake of official copyright, I found this image on the web, linked and copied many times, but Gary Larson and his publisher own all rights to the image. I am just passing it along for the humor value.

Why am I linking it here? Because in fact it is funny. Any scientist reading the article will realize that the content of the article is distorted, even falsified. The coincidence of the article appearing on the eve of the premiere of "Rise of the Planet of the Apes" movie is ... too good to be true.

Why am I laughing? Because people - especially the press - are gullible. Because I know a few things about how the science is conducted. At present "human-animal hybrids" are not viable. Yes, scientists are looking at genes by inserting a single gene structure into a frog egg or mouse and studying the gene for a better understanding of human disease and medication. At present there is no way to put "animal genes" into humans - after all, where are they getting the embryos? Three universities are named, but not the labs, the people or the specific projects - and that's just not like the historical actions of "whistleblowers" and activists that bring unsafe and dangerous research to light. Someone, somewhere, is laughing at the prank they've pulled on us all.

No. I mean that it was raining. It was daytime, and the rain was warm and gentle. It was a good thing, too, or the stranger would have looked like a ‘drowned rat’.

His fur was black from his head to just above his tail. There was a small patch of white at his throat and at the end of each forepaw. His belly and hind legs were white, giving the impression that he was wearing a tuxedo and tails. “Scoo-bee-doo-bee-doo, bee-doo-bee-doo-bee” he sang quietly as he looked around.

A small black furred head looked out from the back booth. Soon others peaked out from under other booths and one even looked out from the window into the kitchen. The first rat made his way up the the stranger and introduced himself. “I’m Ratley, manager of LabRats, Inc. and supervisor of this crew. What can we do for you, Sir?”

“M’name’s Dean, my good fellow. I seem to have misplaced my Pack and thought I’d stop in for a cuppa Joe.” He looked around at the other rats. "Any chance of that,Sir?"

"Sure" said the large rat. He raised his voice and called back to the kitchen: "Ratso, cup of coffee for the customer!" Turning back, he saw that the newcomer was looking around at the other rats. His gaze lingered on two under the jukebox. "That's YouDirtyRat imitating a dust bunny and Nestor is the one tangled in the electrical cord. Ratso helps out in the kitchen and handles supplies. Ratface is the one chasing his tail and Ratfink is off somewhere up to no good. We're the cleaning and maintenance crew for this Diner. We've also been known to help out with serving."

"And the humans? They *allow* this?" the newcomer asked.

"Sure, ever since Speaker to Lab Animals found us we've been helping out here. The people are nice if a bit strange and we get all the scraps we want. Speaker's that great big human in the booth. He thinks says he's a scientist or something, but he lets us get away from the lab for a bit each day.

"So, what lab are you from, and what experiments have you participated in?" asked Ratley.

"Well, that's a long story" said Dean.

"That's okay, we've got time. It will take the lads a while to carry that cup of coffee all the way out here…"

Friday, July 22, 2011

To explain, let me back up and describe normal activity in the brain: Individual neurons respond to a stimulus by creating an electrical current called an "action potential." This current is caused by a rapid movement of positively charged sodium ions into the neuron from the fluid surrounding it. This electrical activity - called a "spike" or "unit discharge" when speaking of assemblies of neurons - is the essential information carrying actviity of a neuron.

Normally when a neuron generates a spike, neighboring neurons are quiet. This is because a combination of neural connections and neurotransmitter chemmicals at those connections act to block the spikes generated by the nearest neurons. This ensures that the neuron is responding to its own inputs, and not that of its neighbors. It also keeps the representation of information "sparse" to allow a lot of *diifferent* information to be represented.

If the inhibitory connections (using the neurotransmitter GABA - gamma aminobutyric acid) are too weak, the activity of a given neuron can influence or even spread to its neighbors. If the inhibition is too strong, the activity tends to "bounce" or oscillate between active (not inhibited) and inactive (inhibited) states. Either instance can cause neurons within a region to begin firing spikes that are synchronized - all firing at the same time.

This is the essence of a seizure. If the synchronous activity is limited to just a small area, it is termed a "focal seizure" and the patient may experience nothing more than a slight muscle twitch, speech disturbance, visual disturbance, etc. If the synchronous activity spreads, the patient experiences a "generalized seizure" with convulsions and even loss of consciousness. The initial synchronous activity can mimic sensory inputs and cause the patient to "see", "hear" or "smell" something unusual. This "aura" commonly signals to the patient that a seizure is imminent, since it precedes the generalization of seizure activity that leads to convulsions.

If the seizure originates in prefrontal or limbic (hippocampal) regions and does not spread to motor cortex, the patient experiences an altered state of consciousness where they are unaware of and unresponsive to their surroundings - but without convulsions. This is called an "absence" seizure, and can be rather difficult to treat because the symptoms can be easy to miss. Absence seizures are more common in children and youth than in adults; they usually last for less than a minute, and are typically not preceeded by an aura.

Following a seizure, neurons act like any other cells of the body that have had an extreme workout - i.e. they are fatigued. Doctors call the period of a seizure the "ictal phase" and the lethargy, dullness and depression that follows a seizure the "post-ictal phase." In many patients the siezure itself may be undetected (lasting <2 min), and only the post-ictal phase (lasting tens of minutes) is observed.

In many ways, brief focal seizures and TIAs can have similar effects - a transient disruption of brain function that passes in minutes. A key difference is that seizures will tend to always occur in the same part of brain, and the "aura" with seizure onset allows the patient to always predict when an event will occur. Critical to diagnosing the difference between a vascular event and a seizure is the EEG. TIAs and strokes are characterized by a reduction in neural activity while seizures demonstrate an increase and a synchronization simuilar to the EEG shown in the previous blog.

What then, constitutes epilepsy? Is an convulsion or seizure reason to worry about a diagnosis of epilepsy with all of the attendant social issues (fear of seizure in public, loss of driving privileges, etc.)?

No. As mentioned last blog, convulsions can be caused by fever or head trauma and never recur once the fever is lowered or the trauma is treated. Focal seizures without loss of consciousness - especially if preceded by an aura - need not occur with sufficient regularity to warrant medication or treatment. However, recurrent seizure, with altered consciousness, and impairment of thinking, vision, hearing or movement following a seizure *is* epilepsy. Like so many other brain disorders, it represents a continuum from mild seizure to severe, full-body conculsion that can lead to serious injury.

Epilepsy is diagnosed primarily by recorded the EEG from multiple sites on the skull during a seizure. Synchronous firing of neurons in wide areas of the brain signifies an epileptic seizure, and is considered "proof" of diagnosis. Causes of the disease vary, but the consensus is that the "focus" of a seizure (its point of origin) is a region of brain that is predisposed to fire synchronously. Neurologists call this an "irritable" focus, and may indicate that the normal recurrent inhibitory connections which prevent synchronous firing are damaged. As stated before, an irritable focus may result from injury, stroke or disease, and can sometimes be detected on MRI or CT scan.

Treatment of epilpesy and mild seizure disorders is usally via medications that can prevent synchronous firing from developing. Since the medication targets unusual activity, it typically doesn't alter the patients sense of their own brain activity, but if high dosages are required, the patient can feel dull, listless, lethargic or have "fuzzy thinking." Neurologists and pharmacologist have attempted to develop drugs to treat seizures via manipulations of GAB neurotransmitter, but have not been as successful as with other systems. The GABA drugs *do* make good medications for intractable nerve pain, however. If the seizures cannot be controlled with medication, but the "irritable focus" can be accurately identified, it is possible to perform neurosurgery to remove that brain area and stop the initiation of seizures.

The results of such surgeries have been... interesting... to say the least.

Since this blog is now running quite long - I'll stop here and resume next time with "curious things we learned from epilepsy surgery" which should provide plenty of inspiration for the imaginations authors and readers alike!

Stay tuned for LabRat Adventures this weekend and Monday Funnies next week.

Wednesday, July 20, 2011

To follow up on the discussion of stroke and TIA (transient ischemic attacks)... Repeated ischemia can leave scar tissue that is prone to unpredictable electrical activity. The irony is that such unpredictable activity is in fact quite ... synchronized. The EEG traces at right show the random, irregular pattern of normal brain activity at first, then large, synchronous pattern of seizure activity for 5-10 seconds, and a return to normal EEG.

So - what is a seizure?

Most people, upon hearing the term, think of convulsions and epilepsy. However, seizures do not have to involve convulsions, and not all seizures or convulsions indicate epilepsy.

Definitions: A seizure is an episode of periodic, synchronous activity in brain cells that normally do not fire synchronously. A convulsion results from a seizure that involves the motor cortex, resulting in muscle twitches or spasm. Epilepsy is a disease of recurrent seizures - with or without convulsions - that originate in the same area of brain.

Seizures can be one-time events or recurrent - even without a diagnosis or epilepsy. They can be caused by scar tissue from stroke or TIA, from head injury, vascular irregularities, congenital defect or none of the above. Convulsions can result from seizure, infection or fever - anything that causes the motor cortex to fire the neurons out of sequence. A diagnosis of epilepsy generally only comes once seizures are diagnosed as recurring uncontrollably, do not respond to baseline medications, and involve an altered state of consciousness. In this manner, tics, spasms, tinnitis and optic flashes are all forms of seizure (if they originate in the brain) with no stigma of epilepsy involved.

Convulsions come in many different types - the petit mal seizure evokes hardly any muscle twitch, while the grand mal can involve muscle spasm throughout the whole body. Partial seizures may involve a single limb - right hand and arm up to the elbow, for example - or perhaps part of the face. Complex seizures progress from one area of the brain to another - thus producing a "march" of convulsions until they involve the whole body. [A "complex-partial" seizure starts as a partial seizure - generally involving a single limb, then progresses to whole body convulsion.]

The next blog will complete the discussion by exploring the various forms of epilepsy, with discussion about medication, diagnosis and the lifestyle impacts of seizures.

Monday, July 18, 2011

After much consideration of the amount of time I had available to prepare blogs, as well as what direction I wished to take this blog when The Guide is finished, I have decided to change up the posting schedule. I had the great good fortune to attend LibertyCon this past weekend in Chattanooga this past weekend. I participated on Science panels, spoke at length with many authors, and with the inestimable Pete Abrams, creator of the long-running "Sluggy Freelance" webcomic (http://www.sluggy.com). Among other things we spoke of science and webcomics. It occurred to me that this blog would be a good place to link to stuff that makes me laugh - as a Scientist!

The Classic example of Science Humor is the sadly no-longer-drawn Far Side comic. Gary Larson just had a way of poking fun at Science and Scientists while still capturing the essence of what makes us tick. It is still around in calendars, web links and taped to walls of student cubicles and academic offices!

For today, I'd like to link to PhD Comics. "Piled Higher and Deeper" is a phrase quite often used to describe the futility and absurdity of advanced degrees. Jorge Cham's main characters suffer many of the indignities that we all faced in grad school - the distant professor, the unappreciative undergrads, and misunderstanding public. One of my favorite comics describes the "Science News Cycle" (link below) that shows how a grad student's statistical correlation turns into sensational news. Many of us have been there. We have a love/hate relationship with the press and the public. Everyone *needs* to know what we discover, but few of us can have the expository genius of an Isaac Asimov or a Carl Sagan - or even a Jorge Cham.

Saturday, July 16, 2011

This is part two of a four-part series on the interrelated subjects of stroke, TIA, seizures and epilepsy.

In the previous blog, I spoke of strokes - cerebral infarctions which are analogous to the myocardial infarction of the heart (heart attack). Just as the heart has symptoms of angina from temporary interruption of blood flow, so does the brain have TIAs - transient ischemic attacks. TIAs are essentially miniature strokes,without the long-lasting obvious effects of a stroke.

TIAs can result from three factors - (A) low blood-pressure-induced lack of blood flow to the brain, (B) spasm of the blood vessels interrupting blood flow to the brain, (C) breakaway clots that temporarily block blood vessels in the brain. The key feature of all is that they are transient. TYpe A requires two factors - a malformation of blood vessels in the brain that cause the blood flow to be decreased under normal conditions, and an event that further reduces blood flow. The former can be caused by previous blockage, arterial plaques (i.e. atherosclerosis), scar tissue, or malformed vessels. The hypotensive or low whole-body blood flow event can be caused by rapid posture change (usually standing up), using the bathroom (especially if constipated), or medications to lower blood pressure. One example of TIA is thus a person suddenly standing up, getting dizzy, feeling pain, and losing consciousness.

An important issue about blood pressure is that there are two pressure states - the highest pressure is encountered as the heart is actively pushing blood into the highly elastic arteries at the peak of the heart beat. As the heart rests and refills, the pressure in the blood vessels is largely a function of the elasticity of the vessels and smooth muscles lining the vessels which can constrict the diameter and regulate the blood pressure. Thus the high pressure is the result of the heart's ability to pump, and the low pressure is a result of the rest of the circulatory system regulating the pressure via blood vessel size. This minimum pressure is import for being able to force blood through the smallest vessels (capillaries) that provide the actual exchange of oxygen, carbon dioxide, glucose and metabolic wastes at the cells themselves. If there is a partial blockage anywhere, or an area that restricts the blood flow for only a short space, the area downstream will have lower blood pressure and less "perfusion" of blood through the capillaries.

Thus if the whole body blood pressure drops - such as when a person on heart and blood pressure medication stands up suddenly - the pressure downstream from a partial blockage may be too low to perfuse a particular brain area. The neurons are temporarily deprived of oxygen - i.e. transient ischemia - and for a very brief time the patient has symptoms of a stroke - albeit a small one.

A similar temporary occlusions can result from spasm of the smooth muscle fibers that regulate the size of blood vessels. Spasm can be due to drugs or medications, stress, environmental conditions or seizure-like activity (see the next blog!). A vasospasm is also likely to occur if there is an unusual shape or configuration or even damage to blood vessels in the brain. The source can be congenital or due to head injury or even prior strokes.

The final cause is from mobile clots or debris in the blood. The technical term is "emboli" and typical sources include clots due to a damaged heart valve, traumatic injury with extensive bleeding (and subsequent clotting) or peripheral artery disease in which clots form in the legs of patients who have been immobile for too long. Emboli will travel through the blood until they are either broken apart or reach a blood vessel narrower than the clot. If the clot reaches the brain, but once lodged in a vessel it breaks down further, a TIA results. If the clot cannot be dislodged or more clots build up, a stroke results.

TIAs resulting from blood pressure drops or vasospasm may occur anywhere in the brain, but will most likely involve the same area each time if there is a malformed or partially occluded blood vessel that is sensitive to low perfusion. TIAs due to emboli will most likely be different each time since the eventual destination of the clots will vary with each instance.

TIA symptoms vary - essentially they are miniature strokes. Thus the same symptoms of strokes can be applied to TIAs with the exception that they are transient hence the effects may last only seconds to minutes with a complete return to normal function. Some typical TIA symptoms include migraine-like headache that lasts less than 10 minutes, sudden paralysis or weakness that disappears within just a few minutes. Sudden blindness, deafness, aphasia (inability to speak) or incoherent speech that returns to normal before the patient can even seek assistance.

Rarely does unconsciousness result from a TIA, but if it does it may indicate that a more serious condition is developing. Repeated strokes or TIAs may result in scar tissue formation that leads to seizures or even epilepsy. We will begin our coverage of that topic in the next blog.

Thursday, July 14, 2011

This is part one of a four-part series on the interrelated subjects of stroke, TIA, seizures and epilepsy.

Stroke is a common term in today's society. Most of you problem know - or know of - someone who has suffered a stroke. Essentially, a stroke is a same for the brain as a heart attack is for the heart. In fact - they share a common medical name: "infarction." An infarct is an area of dead cells caused by a blocked blood supply. Without blood, the cells have no oxygen, no nutrients, and cannot get rid of wastes. The blockage is usually due to a narrowing of blood vessels due to scarring, plaques or other deposits. In the heart, the blockage grows until it blocks the blood vessel. Blood clots can form at these sites, and may break off and stop at other narrow places "downstream" causing a sudden infarct. Quite frequently stroke is caused by these "wandering" blood clots getting lodged in the tiny, narrow vessels of the brain. Unless the blood supply, and in particular, the oxygen supply, to heart or brain can be replaced or restored, the cells will die.
The picture at left is an excellent illustration - one of the best I've seen to demonstrate a "cerebral infarct" or stroke. The picture is from "The Internet Stroke Center" at http://www.strokecenter.org/education/ais_pathogenesis/13_evol_cereb_athero.htm and I direct readers there for more clinical information.

What you should notice is that an infarct (black) can occur anywhere in the brain - and the dead neurons are downstream from the blockage of the artery. The edges are less affected, since some blood can be delivered via arteries and capillaries (the smallest blood vessels) to the sides. It is difficult to cut off the blood supply to too large an area of brain, because the brain has a highly redundant network of blood vessels (below, left - from The Encyclopedia of Science) at the bottom of the brain. However, as you run out the length of the arteries, you reach brain areas that are served by only one blood vessel - typically these are on the upper surface of the brain, and provide some of the characteristics of a stroke - i.e. loss of motor ability.

Onset of a stroke is typically sudden - a clot breaks loose from somewhere else in the body, travels to brain, and blocks a narrow artery. The brain area "downstream" becomes "ischemic" - meaning it does not have sufficient blood and oxugen flow to keep the neurons functioning. Cells can function for a time without oxygen by breaking glucose down into lactic acid - but without blood flow the glucose depletes, the lactic acid builds up, and then cells begin to die. As neurons die, they release neurotransmitters in such large quantities that they can further damage the surrounding neurons. Unless blood flow and oxygen are restored, an area of brain will die, and that function will be lost.

Brains can recover - somewhat - there is enough redundancy that patients can be trained to recover some function. There is some penetration of oxygen from unaffected areas, and a high oxygen environment is helpful. If the clot can be broken up fast enough, the neurons are damaged, but not dead, and can recover some function. In addition, the brain is remarkably plastic, and functions can switch to other areas of the brain (for example, language and speech have been known to switch from left to right hemisphere!).

The severity and effects of a stroke depend on the location of the infarct. In the Occipital Lobe, an infarct will result in loss of a visual area or even blindness. In the Temporal Lobe, hearing, memory or language capability may suffer. In the Parietal Lobe and the motor areas of the Frontal Lobe, sensory inputs and and motor outputs are the result. Note that the latter are most common because (A) they are most noticeable effects, (B) those brain areas are further from any "collateral" blood vessels that could bypass a blockage, (C) they are survivable. Infarcts in Prefrontal Areas are less commonly noted, because in some areas, there are few obvious effects, except for eye movement and decision making. Also, large infarcts in these areas tend not to be survivable.

More rare would be infarcts of deeper structures, but these tend to have the more interesting effects for a writer: Infarcts of the thalamus and hypothalamus are serious - they affect large areas of the feedback control of the body. Infarcts of the visual and sensory pathways lead to an interesting form of amnesia termed "neglect." In neglect, the patient does not acknowledge that a sensory field exists, even though the body reacts normally to those sensations. In visual neglect, an experimenter can show a picture to one portion of the visual field - the patient is not allowed to move their eyes to "scan" the picture. The patient denies that there is anything in the visual field, but also denies that they are *missing* any portion of the visual field. Yet the rest of the brain knows that image is present - the eyes will track the image, an embarrassing image will cause a blush, etc. The same is true for sensory inputs from the rest of the body. Such effects arise from infarcts at either the inputs through thalamus, or from infarcts in the parietal association areas.

A final note before moving on to the next topic is that some strokes may not be noticeable at all - the area affected may be small, it may be an area with less defined function (i.e. the nondominant hemisoehere of the brain), or they may be so short acting that any damage is temporary. We will cover "Transient Ischmic Attacks" in the next blog.

Tuesday, July 12, 2011

Coming up next: a 4-part series on Stroke, TIA (transient ischemic attack), siezure and epilepsy.

UPDATE 7/13:

Due to a family medical issue (in fact related to the subject at hand) I will need to skip the 7/12 post and run the Stroke, TIA, seizure and epilepsy series on the 14th, 16th, 18th and 20th of July. This will also bracket LibertyCon and allow me a bit of leeway in the posting schedule.

Sunday, July 10, 2011

In years past, the most over-diagnosed psychiatric condition have, in turn, been depression, ADHD, and bipolar syndrome. These days it seems that everyone is talking about Asperger's and Autism. I'm sure that if you are reading this blog you have enough experience online to read comments by posters claiming Aspergers, and seen the web-based surveys that purport to tell you where you fall on a scale from Autism to Aspergers to "neurotypical" (i.e. the rest of us). As I was looking at the potential list of topics to cover in today's blog, my son, studying Forensic Psychology in college, leaned over my shoulder and said "Considering how many people claim to have Asperger's Syndrome as an excuse for being a total jackass - why don't you cover that!"

I have probably lost some readers right there - but believe me - I am not denigrating those with *legitimate* diagnoses of Asperger's syndrome. Instead - I want to make a point about self-diagnosis, which will come a bit later. Way back when I was a Sunday School teacher, I had a 4 year old student that would only play by himself in the corner, he would not socialize, spoke very little and would fight if forced to leave his comfortable spot. He was extremely smart, we could tell that from story time, but he did not socialize well. He had Aspergers - and that was the first I had heard of it. Fourteen years later, he graduated near the top of his high-school class, played in various musical groups, acted in plays and musicals, and was essentially socially well-adjusted - or at least compensated very well.

And the latter point is very important.

Autism and Asperger's are part of a spectrum of disorders characterized by a very poor connection with the outside world. Autism is quite frequently co-diagnosed with hearing disorders - not deafness, but instead a hyper sensitivity to certain sounds. Asperger's and Autism are well defined psychologically, but poorly defined neurologically. In other words, it is hard to point to any one malfunctioning brain area.

This leads to misunderstanding, misdiagnoses, and misuse of the term.

Both Asperger's and Autism have characteristics that show up in scans of brain activity - low activity in the frontal areas, and high activity in occipital and parietal areas - in other words - a lot of sensory activity, but much less "executive function." The exact cause is unknown, but theories regarding insufficient connectivity or hypoactivity abound. There are a few things we do and do not know about the disorders.

Autism and Aspergers are part of a spectrum - at one end are highly impaired persons that do not interact at all with their surroundings - particularly not with other people. At the other end is normal social functioning. The actual description of this scale is "Autism Spectrum Disorder." There can be individuals with ASD that are very bright, very high functioning in society. The only way we know a person might even have ASD is that they don't understand or even detect normal social cues.

Again, there are many popular online web sites and emails that purport to tell you where you fall in the ASD spectrum on the basis of answers to a few (typically <50) questions. SELF-DIAGNOSIS is DANGEROUS! Not to mention notoriously inaccurate. The professional neuropsychological exam that I have seen consists of over 300 questions, several story problems, an interval with a clinical psychologist, and extensive observation of social behavior. Anything less is not a professional diagnosis. Any self-diagnosis is likely to be even less accurate - hence my son's comment in the first paragraph. (Disclaimer he is studying Abnormal Psychology with a minor in Criminal Justice - he knows whereof he speaks!).

We now know that Autism and Aspergers are not linked to childhood vaccinations. The study that reported the link has been proven to be a fraud. The professor stood to profit massively from the resulting backlash against vaccines, and he "cooked the books" with regard to the data analysis.

There are plenty of celebrities that still like to trot out the Autism/vaccine link, saying "Just because that study was disproven doesn't mean it isn't true."

Yes it does.

There was *ONE* study which linked the mercury-containing preservative "thimerosal" with Autism. For the statistics, the author "cherry-picked" 12 subjects out of a base of over 300. Even looking at only 1/25th of a population of persons with autism, the statistics could *barely* register any cause-and-effect thing over random chance. We now know that even that data was inaccurate, even fraudulent (http://www.bmj.com/content/342/bmj.c7452). The study was disproved, the journal in which it was published has retracted the finding and censured the author - but does that mean the data says otherwise?

Yes, the data says otherwise. An article by Stehr-Green, Tull, Stellfeld, Mortenson, and Simpson: "Autism and thimerosal-containing vaccines: Lack of consistent evidence for an association," appeared in the American Journal of Preventive Medicine, Volume 25, Issue 2, August 2003, Pages 101-106. (DOI: 10.1016/S0749-3797(03)00113-2) (http://www.sciencedirect.com/science/article/pii/S0749379703001132) This study shows that the rise in Autism diagnoses predates the rise in mercury content of vaccines in California, and is parallel in Sweden and Denmark, countries with negligible Thimerosal/mercury exposure.

The link between Autism and vaccines has been disproved. Before believing any celebrity that says otherwise - ask yourself first whether, since even supposedly credentialled science can be false, do you really trust an uncredentialled musician, actor, politician - or even writer - to practice medicine without a license?

So - how to incorporate Autism or Aspergers as a plot device?

It would be very difficult to write a primary character with ASD - we just don't know the neurological basis for the disease. On the other hand, we know that patients with ASD need extra parental care and different social encounters - it would be a perfect plot device to include an Autistic or Asperger's relative to explain a protagonists busy - even hectic - life and strained social relationships.

Friday, July 8, 2011

I was once asked: "could someone please give me a precise definition of ADD? i've gotten a pretty good impression from various online discussion posts, but i'd like a more accurate explanation."

"Precise is, of course a relative term, but here goes..."

ADD is a condition of the brain that affects the ability of a person to shift and apply the focus of their attention. The popular observation of ADD is the "MTV" or "Sesame Street" kid whose attention cannot be focused for more than 5 minutes on any one thing. This is not entirely true, since many kids under 10 would be hard-pressed to concentrate on a boring task for more than 5 minutes anyway.

The key is to "shift and apply" the attention. ADD individuals may be able to "hyperfocus" and shut out all external stimuli, as long as what they are focusing on holds their interest. If you try to break their attention away and cause them to do something else, they may resist to the point of a temper tantrum (even adults). On the other extreme, if the task at hand is not interesting to them, their minds will skip and flit from subject to subject just like a channel-surfing TV watcher, unable to find anything to stimulate their interest.

Clinically, ADD centers around areas of the brain that affect attention, satisfaction and pleasure. The current thinking in the physiological end of the Neurosciences is that there is too little activity of the attention centers of the brain (including the "reticular activating system" right), and the patient cannot focus. This is a chemical disorder, and can be treated medically. In later ages, the ADD person can adopt "thrill-seeking," "self-destructive," or substance abusive behaviors in the attempt to find the stimulation that will help focus their attention. In children, the temper-tantrums and misbehavior so often associated with ADD may be another form of seeking stimulation from their environment.
ADD is NOT:

simply misbehavior

the result of too much refined sugar (my mother's favorite, circa 1971)

hyperactivity (although there is a combined ADD/hyperactivity disorder termed ADHD.)

depression (although both clinical/biochemical and psychological depression can quite often accompany it.)

unusual

a catchall term for kids that the adults are uncomfortable with

sssociated exclusively with high or low intelligence

A note on #5 above: ADD and ADHD can be reflected in a continuum of behaviors, with 0 as a "normal" person who can shift attention easily, yet will focus on even the most ***boring*** task with no trouble, to 10 as an ADD child who can't finish a sentence without running off to do something else (and changing their mind before they get there). It would be more fair to place a majority of persons in the 2-7 range, with the clinical ADD condition (requiring medication) starting at about 6.

A note on #2 above: There is as yet no good reliable link between diet and ADD. There is some link between lack of protein in the evening meal and insomnia (and hence the bedtime behavior of ADD kids), but there is no justification for holistic or homeopathic cures for ADD. Keep this in mind. Any cure can work for *you* if you believe in it enough. But *your* belief is seldom sufficient for the person standing next to you.

A note on #3, 4 and 7 above: An elementary school principal of my acquaintance once stated "It's not the smart, ADHD kids I worry most about, they can be helped by medication and also in part by enriching the classes and giving them challenging work. I care about them, but I worry most about the true ADD and depressed kids. (NOTE: ADD - not ADHD - kids are often lethargic or hypoactive.) They can be so 'out-of-it' not paying attention and yet not making trouble, so that you don't pick up on the problem until it has progressed further than with the other kids. I worry that we can be doing these kids a greater disservice."

Now, I'm not going to tell you how to determine if a child (or parent) has ADD or ADHD. That job is best left to the professional clinicians. BTW, they need to know the patient's history. As has been stated elsewhere, a history of ADD/ADHD symptoms before age 7 is an important indicator.

I've heard parents (including myself) say: "My kid can't have ADD, (s)he can sit for hours watching SpongeBob!" That may or may not be true. What does it take to *break* their attention away from the tube? ADD is almost as often reflected in the inability to *break* attention as it is to focus attention.

ADD is sometimes referred to using the term hyperfocus, the ability to selectively focus attention to the point that *all* distractions short of earthquake, fire and flood can not cause the attention to be broken. In terms of the mechanisms of ADD, the scientists feel that since the patient has an underactive system for regulating attention in the brain, anything that *does* activate the brain will be reinforced and the patient will try to maintain that stimulation as long as possible. Of course with the 7 y.o. child, when you force them away from this stimulation, they'll fight you... kicking, screaming, ... in public, preferably.

Is ADD overdiagnosed? I don't know. Is it better *understood* so that doctors are more apt to correctly diagnose it and treat it accordingly? Definitely.

What about medication? In short, it works. Ask any parent of a well-treated ADD child. It seems paradoxical: in the 60's and 70's we referred to the fact that it was strange that stimulant drugs actually calmed down hyperactive kids. However, the commonly used stimulant, Ritalin (methylphenidate) acts directly on the attention centers of the brain. The effect is similar to the "squelch" on a CB radio (remember those?). By increasing the separation between signal (attention) and noise (distraction), you allow the patient to focus appropriately without resorting to the hyperfocus that causes problems. You really should see my son doing homework these days, or sitting quietly in a department store watching the people.

I've heard complaints from teachers and parents alike that we are:

teaching our children to be drug addicts,

treating them with *too harsh* a chemical for developing brains,

teaching them to rely on a crutch rather than learning discipline and self-control.

As a professional neuroscientist with experience of both physiology and pharmacology, I respond:

Methylphenidate is not addictive in the classical sense. Despite a *superficial* chemical resemblance to cocaine, as well as some reports of a "high" induced by massive doses, methylphenidate has been shown *not* to produce craving or withdrawal even at those massive doses. Methylphenidate will *not* support a "self-administration" behavior in the laboratory -- a well accepted scientific model of the addictiveness of a drug where a lab animal (rat or monkey) or human can "choose" whether and how often to take a drug.

A 10-year-old's metabolism is *considerably* different than an adult's. In addition, the reaction of a non-ADD adult to Ritalin bears *no* comparison to that of an ADD child. Many of these drugs are *more* harsh to the adult with the altered metabolism that comes with age, alcohol consumption, nicotine consumption, onions, pickles, jalapeno peppers! Also, if your brain does not need the boost to its attention mechanisms, the effects of the drug will be felt elsewhere.

The goal of medicine as a practice is to improve the quality of life of the individual. If giving an ADD patient Ritalin improves their ability to function in society, shouldn't that be our goal?

..and breaking character for just a moment: "As a parent I respond: YOU COULD MAKE THE SAME ARGUMENTS ABOUT INSULIN! Would you deny insulin to a diabetic child? Or would you deny a crutch to person with a broken leg? The tool (not a crutch) is there to help us learn to live our lives without also having to fight past an otherwise incapacitating condition."

Now, back to the objective descriptions, and here's where the usage of ADD/ADHD as a plot device comes in: ADD can be diagnosed at any age. There are adults with ADD or ADHD. Quite a few medical students have it. Many adults of your acquaintance can probably also confirm it.

There are typically three groupings:

Children diagnosed with ADD who require Ritalin until their teens. Either their brain chemistry changes or they had milder conditions that allow them to learn coping strategies (sort of like dyslexics learning to read).

Children diagnosed with ADD that require Ritalin well into adulthood.

Adults that were never diagnosed with ADD as children, but find that so much of their behavior fits the descriptions of ADD/ADHD that they can be helped with Ritalin. These individuals might have shown severe ADD symptoms as kids, but their parents resisted medication, or they may have gone undiagnosed. It is less likely that the ADD just *appeared* as they grew older. Others have been known to say "I always thought something must be wrong with me, but I never knew what until now."

ADD can be masked by or show up in conjunction with depression. That was the case with my own son. Many of the severe issues we faced with his ADHD (diagnosed at age 7) were confounded by increasing moodiness and argumentativeness. At age 15 the psychiatrist diagnosed depression (although to be fair, there were indications at age 7, but he had just suffered through death of his grandfather, so it was not considered clinical depression at the time). The addition of antidepressants (and Prozac is still the only antidepressant approved for use in patients under the age of 18!) helped a lot, and by the time he entered college he was completely off of all medications. It was rough, but he made it - he's self motivated, choosing his career and made Dean's List last semester.
By the way, if you are looking at this in terms of personal application, and not just how to incorporate in a story, have a friendly talk with your family physician. I am in the business of training doctors, and the importance of good doctor-patient communication cannot be stressed enough. If you don't trust your doctor, talk to another doctor. If your doctor doesn't communicate well with you, tell him or her that you don't feel you are getting sufficient information, and *ask* for better communication. If you don't get it, find another one. Start at the personal physician stage, and then go to the specialist: psychologist or psychiatrist. If you can't get a referral, talk to another doctor! (Get the point?) If finances are tight, call the local AMA or medical association, or call a medical school. See if someone will talk to you without the full office visit charges. But most important *!*!* ADD should be diagnosed by a qualified professional in a clinical setting, not over the internet, and not from reading Psychology Today.

O.K., that's the summary. ADD is pretty well defined, and pretty well treated.

As a final point on writing about ADD and ADHD, keep in mind that some folks can do well without medication, but are so much happier when they have it. From my own experience, I know that my son was quite unhappy to *know* he was getting in trouble and couldn't really control it. He loved to do a lot of different things (reading, composition, soccer, basketball, art) which he didn't do as well without medication (especially writing compositions). So, if writing a character with ADHD, try to explore some of the consequences of nottaking the medication - fuzzy thinking, lack of attention, inability to complete a project, then compare to the capabilities when on appropriate medications. Explore different variations: Perhaps extreme heat or exercise causes the medication to wear off too quickly, or the meds interfere with sleep (they can, if too much is taken too late in the day). With an appropriate background, you can make the character more "real" to readers who have been there, and done that.

Until next time, don't just take care of your brain - use it and write it with care!

Wednesday, July 6, 2011

The new chapter of The Lab Rats' Guide to the Brain is all about diseases and disorders of the brain. Since this is a guide to writers (as well as readers), some attention will be paid to how to describe and use these disorders to further a story or to provide an interesting background for a character.

For example, the suspense author Dean Koontz has had protagonists with extreme photosensitivity, Asperger's Syndrome, or been blind. The story is not about the disease or disorder, but the consistency of the characters actions within the context of the disease/disorder are what make the character real, sympathetic, and make the reader care about what happens to the character.

This new section will lead off with a discussion of Attention Deficit Disorder and work through the following list:

I would also like to have reader questions and suggestions that will be blogged under the heading:

Dr Welby and Dr. House's "Disease of the Week"

These should be questions about "unusual" diseases and disorders and can include general discussion of how popular media likes to latch onto unusual and bizarre medical cases. If you don't get the TV references, Marcus Welby, M.D. was a TV show from the 70's which featured a kindly family practitioner who was sort of a "kindler, gentler" as well as more accurate version of today's "House, M.D." Dr. Gregory House employs a Sherlock Holmes approach to rule out 2-3 misdiagnoses (much to the detriment of medical and scientific accuracy) before discovering that the patient was "bitten by the rare blue-bottle fly in a particular Louisiana bayou under a full moon, and has thus developed an even more rare foaming blood disease!"

Monday, July 4, 2011

For the last several months this blog has discussed brain science in some detail. It is fairly easy to do. I get questions, I write a description, you give me feedback. But for the most part, I do not see you and you do not see me. It is a rather anonymous relationship, aided by the fact that I write with a nom de plume to isolate my ramblings from official proclamations that could be attributed to my professional day job. I am ethically constrained from "practicing medicine without a license." Likewise I must make sure that nothing I say could be construed as an official communications or positions of my employer. Even when my super-secret pen-name identity gets frayed around the edges, it's still plausible deniability.

It's not so easy in person.

Scottish Highlands

During my recent trip to Scotland I was frequently asked what I did. This was usually by folks either at my destination or traveling with me on the airplane or train. An American going to Aberdeen Scotland is frequently assumed to be in the oil business. Aberdeen is on the North Sea and a convenient dispatch point for the oil rigs. Folks are then quite surprised to find that I am an academic, a professor visiting the medical school.

"What do you teach?" is the frequent question. I tell them I mostly do research on Learning and Memory.

"Oh, I need some of that!" is the response *so* many times that I have lost count. I usually laugh and say that I do to, hence the reason I do the research.

Occasionally someone will probe deeper, and I will mention that some of my work involves drugs of abuse that alter memory. It's a fairly safe topic and I can talk about it fairly easily. I stay away from discussions of drug legalization, I don't mention neural prosthetics, and I especially don't talk about the use of animals in research. I *can* and will, but in Europe and the U.K., it's not something I'll discuss in a public place. Many years ago I was in Austria for a meeting when some exciting scientific news was released about a drug that counters the memory impairment accompanying sleep deprivation. When discussing it with some U.K & European students and postdocs, I was informed that (A) Sleep deprivation is an American problem, people really should just sleep more,(B) Americans have no respect for the rights of lab animals (the drug was tested in primates) and (C) We Americans should just hope that the military doesn't get hold of the finding, since they would only abuse it.

The ignorance and anti-science bias of these supposed scientists-in-training was astounding! How much more so would we find public attitudes? One need only to look at the comments to a recent New York Times review of a scientific journal article by some of my colleagues (http://community.nytimes.com/comments/www.nytimes.com/2011/06/17/science/17memory.html). Since I am interested in, and know the work by these folks, I know that many of the news articles got subtle details wrong or overstated the findings - still the public attitude was about 50:50 supportive and ignorant - ignorant of the findings, ignorant of the applications, and ignorant of the essential value of scientific research.

I blame media: I blame news that will report only sensationalized stories. I blame movies and TV that portray scientists as evil monsters or overlords bent on world domination. I blame Science Fiction that often gets scientific details wrong.

I blame our educational system that "dumbs down" science for the least common denominator. There are schools in inner-city Los Angeles that teach only one week of science in the entire school year. Students get to college and still have to take more than a year's worth of "general education" or "liberal arts" classes to make up for what they didn't learn in grade school, then require 5-6 years to get a 4-year education. We have graduate students in science that can't write - heck we have *professors* that can't write!

I blame politicians and public figures that will latch onto a single scientific "fact" and never let go even when it is proved to be wrong. It is now clear that the "fact" that measles vaccinations "caused" autism was wholly manufactured by a "scientist" with inadequate credentials, inadequate research, inadequate statistics, and who stood to personally profit from the public panic caused by his pronouncement. Yet we have celebrities and public figures who will state that "just because that piece of evidence was disproved doesn't mean it isn't true!" Why, yes it does, but ignorance of science means you don't understand *why* you are wrong. Further, the politicization of science means that dissention and research into alternatives is shut down as being not "politically correct."

I blame scientists.
Yes, I do. We avoid publicity, because we don't want to be targets. We are not taught to speak to lay audiences, we don't give good interviews, we don't write for the general public. We couch our papers in terminology and equations that can only be understood by others in our (very) restricted fields.

I recall a "Wizard of Id" cartoon in which the wizard is complaining that athletes earn more than scientists. He is told that no one ever bought a ticket to see a scientist!

It's true. We're boring. Science is not bubbling flasks of colored liquids, flashing lights or sparks of lightning. The lab rats are in cages and not mutating into city-destroying monsters (except for Ratfink). A "mutant" in real scientific terms has one gene changed, leading to something as benign as more or less sensitivity to a particular drug. Science is grad students in the lab all day and night looking through microscopes. It is professors sitting in front of a PC running statistics and writing grants and papers. It is researchers spending hours or even days soldering, clipping and connecting wires to get another 25 microvolts of noise removed from their recording systems.

So what can we do about this?

You're doing it right now, as am I. Science needs to be brought into the public eye. *Real* science: accurate, precise, and understandable. Writers like Asimov, Sagan and Crichton who write fiction and nonfiction from the perspective of a scientist. SF writers Catherine Asaro, Travis Taylor, Stephanie Osborn, Gray Rinehart - and yes, Tedd Roberts - who *are* engineers and scientists and write SF with real science in it.

Scientists need to talk more, interview more, and frankly, write their science in a manner that can be understood by the public. We need to *teach* science, and debate it openly in public without anyone shutting one side down as being a foregone conclusion.

And those of you who are writers, or want to be writers: get the science right.

---

This blog has covered all of the basics of the brain, structure and function. Next we need to discuss using this info in writing, and the best way to do that is to discuss specific brain diseases and disorders and how to incorporate them as plot devices.

I'll put up a brief post on Wednesday outlining the upcoming topics, as well as an invitation to readers to suggest topics or questions, then Friday we'll start to dig in. If I have to change the blog posting schedule to accommodate day job and blogging, I'll make that announcement next weekend.

Saturday, July 2, 2011

I am a people watcher. OK, I admit. I'm male, I watch the girls - but still I watch everybody. I sometimes try to guess their professions, where they come from, what they like or dislike.

Sometimes they make it easy for me.

Suits.

I'm sitting in a lounge overlooking Paddington Station. It's nearly 8 PM and there are still businessfolk heading home. Perhaps they've stopped for a quick pint at the Mad Bishop and Bear.

The suits are easy to categorize - they work in an office. But what kind? I imagine the lawyers are straitlaced, their collars still buttoned and ties still tight even at this late hour. Ad agency executives will surely have loosened theirs by now.

Young lady in jeans, T-shirt, carrying a backpacker's pack that is almost taller than she is. Student? Tourist making their way across the hostels of Europe?

Ah, now there's a set of interests that advertises itself - young man in a T-shirt for a band. Name not recognizable to me, but the pattern is familiar. Not like the one I just saw in the airport last week: something on the lines of "New York I there." Yup, several words must be missing from that one. The three men appeared to be either "futbol" or rugby players. Accents were eastern European.

Mohawk!

Speaking of exclamations, the greengrocer's apostrophe has nothing on "Yo! Sushi" Yo! advertises "Fresh! Japanese! Food!" Do you suppose the exclamation marks enhance the freshness?

Ah. American tourists. Mom, Dad, two kids. Son wearing a "Texas" sweatshirt, being reined in by mom. Sure, they could have recently toured the U.S. or have a relative in the Great State, but everything about them screams "American!" (see those exclamation points *are* useful). I can't really define it, but I am sure that people say the same when they look at me - especially when I brought *my* family with preteen sons to the U.K. in 1998.

Then again, maybe they just came from The Texas Embassy (restaurant and pub) in London. By the way, I have since learned that I am not really in London. I am in the City of Westminster. London is more an *honorary* name for the metropolitan area. It's historical.

Yup, here comes a party in the making - four women, three men - guys in casual wear, gals in evening dress. Wow, I didn't know they made that in all leather - must have been a small cow, since it's not all that *much* leather... Another in a short dress with shiny full length zipper - looking kind of wobbly on five-inch heels. The group went into Sainsbury's (grocery) and came out carrying bottles. Someone's planning on having a good time tonight.

Here comes a tour - it must be. About a dozen young boys with backbacks and small bags, four adults. Looks like the group that my son was in when he toured Rome-to-Athens with a school tour at age 12.

Oh my.

Gulp.

That was... amazing.

I *really* wouldn't have been sure I saw that if it wasn't confirmed by someone else saying "Did you see that?" I can't do this justice, but... inflatable man doll being towed through the station - a crowd of women, maybe 8 or 10 of them, all with those short wheeled bags that the airlines call "rollerboards" (from the "Roll-aboard" trade name). They are in their late 20's, early 30's in age, one of the ladies was wearing pink, fluffy bunny ears and some kind of sash. A-Hah! I get it. It's a hen party. The sash reads "bride-to-be." I subsequently saw another such group - all in pink T-shirts, pink shoes and boots, and pink cow-girl hats - again, one of them had "girls-on-tour" and "bride" on her T-shirt. Mr. Inflatable at least has some briefs on, but it's clear he has more to Tweet about than Weiner.

More business travelers - the serious ones in suit and tie - the casual businessmen in just a dress shirt, or jackets with no tie. There *is* a tie shop in the station, for those guys who either realize they *need* one, or maybe for those who spilled their noodles at lunch and need to look spiffy for the afternoon meeting.

AUUUUGGGHHH! My eyes! Too much Spandex! *Some* women just should *not* wear spandex - at least not without reining in those love handles.

I am rather surprised at the number of folks wearing headphones - not earbuds - headphones, full over-the-head-cup-the-ear headphones. Mostly guys in T-shirts, a few young women.

Backpacks, day packs, duffles, rollerboards, full-sized suitcases. This *is* the major rail gateway to Heathrow Airport, after all.

Now *here's* drama: A man being led out of the station - security in the yellow vest in front, two women in dark suits (plainclothes? Rail employees?) one on either side with a firm grip on his arm. Oh! He's handcuffed. As he disappears from view, two police come rushing down from an upper level and chase in the same direction.

Wow. You can *not* make this stuff up! What a boon to an aspiring writer.

Now that I've got the writing done (3 grant applications, two papers and a major project review all complete in 4 weeks! Woo hoo!) I have my eyes open and am shifting my brain into writing mode.